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spk08: Thank you for standing by, and welcome to the CINDAC's first quarter 2021 earnings conference call. At this time, all participants are in a listen-only mode. After the speaker presentation, there will be a question-and-answer session. To ask a question during the session, you'll need to press star 1 on your telephone. Please be advised that today's conference is being recorded. If you require any further assistance, please press star 0. I would now like to hand the conference over to your speaker today, Melissa Forrest of Argo Partners. Please go ahead.
spk04: Thank you. Welcome and thank you to those of you joining us on the line and the webcast this afternoon for a review of syntax's first quarter 2021 financial and operating results. With me this afternoon to discuss the results and provide an update on the company's progress are Dr. Briggs Morrison, Chief Executive Officer, Daphne Caritas, Chief Financial Officer. Also joining us on the call today for the question and answer session will be Michael Metzger, President and Chief Operating Officer, Dr. Michael Myers, Chief Medical Officer, and Dr. Peter Ordentlich, Chief Scientific Officer. This call is being accompanied by a slide deck that has been posted on the company's website, so I'd ask everyone to please turn to forward-looking statements on slide two. Before we begin, I would like to remind you that any statements made during this call that are not historical are considered to be forward-looking statements within the meeting of the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these statements as a result of various important factors. This includes those discussed in the risk factor section in the company's most recent quarterly report on Form 10-Q, as well as other reports filed with the SEC. Any forward-looking statements represent our views as of today, May 11th, 2021 only. A replay of this call will be available on the company's website following the conclusion of the call. And with that, I'm pleased to turn the call over to Dr. Briggs Morrison, Chief Executive Officer of Syndex.
spk01: Great. Thank you so much, Melissa, and thank you to everyone for joining us on today's call in the webcast. Slide three provides a high-level summary of our current corporate priorities as we strive to realize a future in which people with cancer live longer and better than ever before. We've continued to make great progress in both our clinical programs during the first quarter of this year. We reported the initial data from the phase one trial of SNDX5613, our selective Mennon inhibitor, and are on track to begin potential registration cohorts in that program shortly. In addition, we have completed enrollment of 23 chronic graft-versus-host disease patients on axotilumab at one milligram per kilogram in our Phase II expansion cohort, and enrollment is ongoing in our pivotal Agave 201 trial. We therefore remain on track to have two registrational programs ongoing this year for two first-in-class and potentially best-in-class medicines for two areas of important unmet medical need. Thanks to the support of our many committed investors, we are well financed to vigorously pursue both of our existing programs and to aggressively look for additional opportunities to bring targeted oncology drugs into our pipeline. Let's now turn to slide four in our recent data disclosure of our phase one trial of 5613, our selective menin inhibitor for the treatment of acute leukemia. As we noted in our recent data disclosure, in our phase one trial, 5613 has been well tolerated over multiple cycles with no patient discontinuing for a drug-related adverse event. Our pharmacodynamic data confirms the mechanism of action, and perhaps most importantly, we have a candidate recommended phase two dose that meets all of our pre-specified criteria. We are, of course, excited to have also observed clear evidence of monotherapy activity in this population of patients with relapsed or refractory acute leukemia with both MLLR and NPM1C mutations, with most responses being MRD negative. I want to reinforce why we are so excited about what we are seeing and provide additional data that further builds our confidence in our program. Let me first remind everyone that this is a phase one trial. Patients have received on average three prior therapies. About 40% had relapsed after a bone marrow transplant. a very negative prognostic sign, and almost 60% had previously received venetoclax. These are very difficult to treat patients, and we were delighted to see a 48% overall response rate and 67% of the responses being MRD negative. Every physician currently treating acute leukemia who has reviewed this data with us has been excited by the efficacy we are seeing. And the data has only gotten better over the past weeks with two patients converting to CR with full count recovery. We had pointed out that it is not uncommon for patients with complete eradication of leukemia to initially have incomplete recovery of their additional blood counts. Full recovery can take time. Slide five is a reprise of one of the vignettes we presented at our data disclosure event. You will see here a patient with refractory NPM1C acute leukemia who was treated at our recommended phase two dose and had a rapid MRD negative CR. Initially, however, her blood counts had not recovered to normal and she had a CRI, which is an MRD negative complete response with incomplete recovery of her blood counts. But you can also see that over time, her blood counts fully recovered She had an MRD negative CR with full count recovery and went on to potentially curative bone marrow transplant. At the time of our data disclosure, we noted that five patients had already achieved either a CR or a CRH and that there were five patients still ongoing who had an MRD negative CR but had not yet achieved a CR or CRH. We anticipated that some of those patients would have full count recovery over time, and that's exactly what we have seen. Over the ensuing weeks, two of the patients who had an MRD negative CR but had not yet achieved a CR or CRH have now had full count recovery and now have achieved a CR and remain on study. A third patient of the five who had an MRD negative CR but had not yet achieved a CR or CRH, has improved from a CRI to a CRP, and also remains on study. Of the two remaining patients, one remains on study with a response of CRP, and one is off study due to progressive disease. Slide six shows the response data we presented on April 20th, as well as the updated data as of last Friday. Let me repeat that these data on slide six are from our ongoing phase one trial. This data on slide six is a snapshot in time and the data may further improve. There are still two patients on trial who have had an MRD negative CR but have not yet achieved a CR or CRH. We are looking carefully at the patient characteristics with respect to any potentially appropriate adjustments to our enrollment criteria in our upcoming phase two study. we understand the regulatory precedent for the efficacy hurdle for the approval of 5613 in relapsed and refractory acute leukemia. While there are no guidelines on a specific rate that is required for approval, we have pointed out the rates that were reported for recently approved FLT3 and IDH inhibitors that suggest the CR plus CRH rate above 20% has been acceptable to the FDA. The Phase 1 data that we've generated from our ongoing Augment 101 trial, and again, I want to emphasize it is our data that gives us confidence that 5613 will achieve that level of efficacy in our upcoming Phase 2 trial. I also want to provide a broader context about what we are seeing in the NPM1 population, as we believe it's quite informative and supports our confidence that the efficacy in the NPM1 population should mirror that of the MLLR population. For the avoidance of doubt, we reported that we had treated seven relapsed or refractory patients with NPM1C acute leukemia, and there were two patients with a CR. Of the remaining five patients, one progressed quite rapidly on the third day of treatment, and two had clear evidence of anti-leukemic activity, but unfortunately succumbed to a systemic infection one of the feared complications of acute leukemia prior to attaining a bone marrow response. So we believe the fatality of our clinical data suggests therefore that as predicted from the preclinical data, 5613 will have good activity in patients with NPM1C acute leukemia as well. Slide seven shows our go forward plans for 5613. We anticipate initiating phase two at the end of this quarter. and holding our end of phase one meeting with FDA shortly thereafter. We also anticipate a further update of the Augment 101 data at the end of this year, and we'll of course also look for additional opportunities to provide meaningful updates as events allow. The phase two portion of the trial will enroll three distinct expansion cohorts, patients with MLLR acute lymphoid leukemia, ALL, patients with MLLR acute myeloid leukemia, AML, and patients with NPM1 mutant AML. The Phase 2 portion will enroll both pediatric and adult patients, thereby providing us a potential path to regulatory approval with a broad label including both adults and pediatrics. I should note that the results are positive. This Phase 2 portion of Augment 101 could potentially support a regulatory filing given existing regulatory precedents. We do not yet have a final endorsement of our phase two sample size, nor have we finalized our enrollment rate, and yet it is possible that we could have top line data for one or more of the cohorts sometime next year. Over the last period, we've also been conducting extensive research into the broad landscape of clinical opportunities for 5613 beyond the initial approval in relapsed refractory acute leukemias as illustrated on slide eight. We are not in a position today to lay out the specific next steps in building out the 5613 franchise. I can say that we are using this ongoing analysis to inform specific combination regimens that we anticipate starting to study later this year. Several investigators and leading companies have already reached out to us with novel, exciting ideas for future development of 5613, and we are evaluating those opportunities. Let me now turn to slide nine and axotilamab, our potentially best-in-class monoclonal antibody targeting the CSF1 receptor. As you know, we presented our phase one chronic graft-versus-host disease data at ASH in December of last year. You may recall that we had opened a phase two expansion cohort at the one milligram per kilogram dose, and we are pleased to announce that that cohort has now been fully enrolled. We anticipate presenting later this year the full updated data from both 17 patients from the Phase 1 portion of the trial, as well as the 23 patients enrolled in the Phase 2 expansion cohort at the 1 mg per kg dose. I should emphasize that our base assumption is that this 1 mg per kg dose will be our labeled dose, and hence the Phase 2 expansion cohort is quite relevant as a de-risking event to the eventual outcome of our pivotal trial. Slide 10 outlines our pivotal trial for axotilamab, a chronic graft-versus-host disease. This trial is the axotilamab for graft-versus-host disease trial called Agave 201. This trial is enrolling patients with chronic graft-versus-host disease whose disease has progressed after two prior therapies. Patients must be at least six years of age and have met overall entry criteria. This is a pivotal dose-ranging trial in which patients will be randomized to one of three treatment groups, each investigating a distinct dose of axotilamab given either every two weeks or every four weeks. The primary endpoint is overall response rate using the 2014 NIH consensus criteria for chronic graft-versus-host disease. Secondary endpoints will include duration of response and validated quality of life assessments using the Leigh symptom scale. Enrollment to the study is underway, and we are on track to deliver top-line data in 2023. We believe that chronic graft-versus-host disease represents a high unmet medical need and an important commercial opportunity, with approximately 14,000 patients suffering from chronic graft-versus-host disease in the U.S. today. With the recent positive pivotal results from both Insights Jackify and CADMINS KD025, we may soon see regulatory approvals and commercial launches that will begin to delineate the commercial opportunity in chronic graft-versus-host disease. Despite recent advancements in this area, to our knowledge, axotelimab is the only agent in clinical development that specifically targets the monocyte macrophage lineage. We believe the data generated to date with axotilumab suggests that it has the potential to play an important role in the treatment of chronic graft-versus-host disease, both as monotherapy and given its safety profile, potentially in combination with complementary medicines. We've also been working extensively with experts in the field of fibrotic disease, and have found a strong consensus that the scientific rationale for the efficacy of axotilumab in chronic graft-versus-host disease firmly supports its potential in a wide variety of fibrotic diseases, such as idiopathic pulmonary fibrosis and scleroderma. We are actively evaluating options by which to build the axotilamide franchise beyond chronic graft-versus-host disease and take advantage of what we believe are a significant set of opportunities that could materially enhance shareholder value. As we have previously communicated, we obtained orphan drug designation from the FDA for the use of axotilamide in IPS. Finally, slide 11 summarizes the transactions that led to the acquisition of the MEDIN MLR program and the Axotilamab program. We believe that we will be able to continue to expand our pipeline through the acquisition or in-licensing of quality, differentiated assets. We believe that we have the necessary skills to evaluate and identify high-quality assets and the clinical development experience to bring these compounds through valuable inflection points. We expect to remain among preferred partners of such transactions. I will now turn the call over to Daphne to review our financial results.
spk03: Thank you, Brig. The results of our operations for the first quarter of 2021 and the comparison to the prior year quarter are included in our press release, so I won't repeat them in these remarks. Additional financial details are available in our first quarter report on Form 10-Q, which was filed earlier today. I would like to point out that our net loss for the quarter was $27.7 million, or 54 cents per share, compared to $19.1 million, or 56 cents per share, for the same period last year. Turning to slide 12, we ended the first quarter with $271.3 million in cash and cash equivalents, and 51.6 million shares and pre-funded warrants outstanding. This cash balance provides us cash runway into 2023, and importantly, covers the development costs of both the Axotelimab and the Mennon Registrational Programs to their first approval, as well as provides us the flexibility for continued business development. Looking ahead, I'd like to provide financial guidance for the second quarter of 2021. For the second quarter, we expect R&D expense to be between 30 and $35 million. and total operating expense to be between $35 and $40 million, including approximately $2.5 million of non-cash stock compensation expense. Full year 2021 guidance remains unchanged, and we continue to expect R&D expense to be between $90 and $100 million and total operating expense to be between $110 and $120 million, including approximately $2.5 million of non-cash dot-com expense per quarter. We continue to expect first half expenses to be more heavily weighted than the second half due primarily to the ramp-up in CMC activities for both programs in the first half of the year. With that, I would like to now turn the call back over to Briggs.
spk01: Thanks so much, Daphne. Let me close the call by again noting that we have begun the registrational trial for axotilamab in chronic graft versus host disease and are on track to start the registrational program for 5613 shortly. This management team has been focused on obtaining regulatory approval for drugs that extend and improve the lives of people with cancer. And we consider having two ongoing registration programs as a major achievement. We are also getting increasingly excited about the broad franchise opportunities for both programs beyond their initial registrational indications. We believe 5613 could have broad utility across a wide range of clinical settings in acute leukemia, and axotilumab could represent a broad franchise opportunity in fibrotic diseases. We are comfortable, given our cash on hand, that we have the financial resources to aggressively advance our programs and achieve key upcoming milestones. We remain optimistic that we can continue to identify and bring in novel molecules to deepen our portfolio. We have a proven track record of delivering on this pillar of our strategy, and I believe it is a core strength of our company. As always, I'd like to thank the wonderfully talented team here at Syndax, our collaborators, and most importantly, the patients, the trial sites, and the investigators involved with our clinical programs. In addition, I'd like to thank our committed long-term investors, who are helping us to build this great company. With that, I'd like to open the call for questions.
spk08: Thank you. As a reminder, to ask a question, you'll need to press star one on your telephone. To withdraw your question, press the pound key. Please stand by until the Q&A roster. Our first question comes from Phil Nadeau with Count & Company. You may proceed with your question.
spk00: Good afternoon. Thanks for taking our questions and congratulations on the progress. First, a clarifying question on the data that you released tonight. In terms of the NPM1 patients and the 29% overall response rate, have you disclosed whether the two responders have had complete hematologic recovery?
spk01: So one of the two NPM1 patients is the vignette that I covered today and was one of the three vignettes that Eitan covered. So that patient clearly had initially a CRI and then had full hematologic recovery, went on to a bone marrow transplant. We have not given any further information on the second patient who had a complete response.
spk00: Got it. Okay. Second question is in regards to the Phase II dose. Many people have noted that recently another cohort was added to the dose escalation study looking at cobicistat-boosting Can you talk about the goals for that cohort and how that plays into your decision on which dose to move into the pivotal study?
spk01: Yeah, thanks for the question. So the cobicisistat arm is really an exploratory arm to look at the effect of cobicisistat on the PK of 5613. It has nothing to do with the doses that we will take into Phase II. We're not waiting for the data from the Covacizostat arm to start phase two. So phase two is the data set that we presented at our data disclosure, so the 226 in arm A and the 113 in arm B. Covacizostat is really, as I said, an exploratory sort of life cycle management study just to look at the PK, the effect of Covacizostat on the PK of 5613.
spk00: Perfect. The last question for Moz, I'm curious if you'd, be willing to address it. I guess the biggest pushback we got after the initial dose was people who were worried that the therapeutic window of 5613 was a bit too narrow, that if you could push the dose just a little bit harder, maybe the efficacy would improve a bit, but perhaps you're somewhat limited by QTC prolongation at higher doses. What's your perspective on that argument? How valid is it, and what gives you confidence that that you're maximizing efficacy at the doses that are acceptably safe?
spk01: Yeah, so as we indicated in the presentation, we had pre-specified criteria for our recommended phase two dose, including exposures that we thought were required for efficacy. We've been able to meet those criteria at the recommended phase two dose. The response rates at the recommended phase two dose are generally the same as what we see in the overall population, which again is not all that surprising since many of the patients in fact were treated at the recommended phase two dose. Again, the vignette I just presented today is a patient treated at the recommended phase two dose had NPM1 disease, a rapid CRI that then progressed to full count recovery. So we feel very comfortable that the dose that we're picking for our recommended phase two dose meets our criteria and that we're not leaving any efficacy on the table by not going higher.
spk00: That's very helpful. Thanks for taking our questions.
spk08: Thank you. Our next question comes from Bert Haslett with BTIG. You may proceed with your question.
spk09: Yeah, I think you just answered it. Thank you for taking the questions and congratulations on the progress. I think you just answered it, but maybe just asked slightly differently. So what then are the specific goals of the interim cohort, the interim dose cohort, and is that a gating item to moving forward into the potential pivotal start on 5613?
spk01: Yeah, thanks for the question, Bert. So, as I just said to Phil, we're very comfortable with the dose, the 226RMA113RB as recommended Phase 2 dose. The investigators and our clinical team wanted to study that intermediate dose to see if, in fact, there was a dose in between the doses we had studied that could also meet our criteria. If those intermediate doses do meet all of our criteria, they could be the doses that we take into Phase II. If they don't, it's not a problem. So those are gating. We do want to wait to get the answer to that question before we start the phase two trial. And again, we feel like we're on track to have that by the end of the quarter. Okay, that's it for me.
spk08: Thank you. Thank you. Our next question comes from Colleen Cousy with Baird. You may proceed with your question.
spk05: Hi, good afternoon. Thanks for taking our questions and congrats on the progress. Thanks for the clarity on the NPM1 patients. I know you noted the two of them succumbed to infection. Did you see any of those in the MLR patients involved in the study?
spk01: I don't remember off the top of my head. I think there was one MLR patient. Maybe Michael Myers, you can answer that question. I think it was one MLR patient who didn't make it through because of an early infection, but Michael?
spk10: Yeah, Briggs, thank you for that, Colleen. Yes, we have seen MLLR patients to have infections. It is an expected complication of AML, especially in patients who have active disease whose counts are not sufficient to protect them from specifically bacterial infections. So as Eitan Stein said in the presentation, Infectious complications of AML are expected and not at all unusual.
spk05: That's helpful. Thank you. And what is the protocol for stem cell transplants in this study, and will there be any changes for the Phase II?
spk01: Well, there isn't a protocol for stem cell transplant in this study. The standard of care is for the treatment of acute leukemia is if you can get a patient into a complete response and particularly if you can get a patient into an MRD negative complete response and the patient is otherwise eligible for a transplant, meaning they have identified an adequate donor, their other general medical conditions are stable, then the patient goes to transplant. So it's the investigator and the treating physician's decision about whether they want to take them to transplant. What they're hoping for is that they can get the patient into an MRD negative complete response, and if so, then they will look to take the patient to transplant. It's not formally part of our phase one study, but it is obviously a very good result for the patients who are able to go to transplant.
spk05: That's great. Thanks. And then for the updated data today, can you confirm, were those centrally reviewed or how were those reviewed?
spk01: So they're reported to us by the scans that you centrally review as you do for solid tumors. So the information is communicated to us by the investigator, and then Michael and his team review the information to confirm it.
spk05: Great. That's helpful. Thank you.
spk08: Thank you. Our next question comes from Peter Lawson with Barclays. May I proceed with your question?
spk06: Great. Congrats on the progress and the update. For 5613, Is there any way of breaking out the CR rate for the, I guess, the 113 milligram go-forward dose?
spk01: Yes, Peter. I think, you know, we're looking for opportunities to present the data at scientific congresses. We'll break out everything by dose and arm. So I think you can look forward to that at an updated scientific presentation.
spk06: Could you disclose if it's above or below the overall CR, CRH rate?
spk01: Yeah, so as I said before, if you look at any of the parameters that we've reported on, overall response rate, CR, CRH, the responses in NPM1, the responses in MLLR, at the recommended phase 2 dose, those responses are generally consistent with what we reported for the overall population.
spk06: Gotcha. Thank you. And then just on the additional arm that was added, just if I could circle back on that, would that be something you'd want to file on with a 6384 kind of onboard, just trying to work through if that's something that gets reported out in two years' time or it's something you kind of have to perhaps use as a go-forward strategy?
spk01: Right. So as I indicated, I think, in Phil's question, It's not a gating item for Phase II. You know, we will proceed with the doses that we've been talking about for Phase II. This is really an exploratory arm as part of our sort of lifecycle management. You know, we are thinking down the road to the point where we get patients in remission who then perhaps in a maintenance point of view, if we can have a greater exposure for any given dose, that obviously decreases the cost of goods, but it's really more of a downstream life cycle as we're thinking about long-term chronic therapy and it really doesn't play a role in the ongoing phase one to phase two transition.
spk06: Gotcha. Thank you. That's really helpful. So it could be in that maintenance setting where you kind of extend the drug into post-therapy. Exactly. Perfect. Thank you so much.
spk08: Thank you. Our next question comes from Justin Walsh with B. Riley Securities. You may proceed with your question.
spk02: Hi. Thanks for taking the question. A couple of months ago, a competitor announced that it's using MRD-CR as a primary endpoint for its drug in newly diagnosed NPN1 mutant AML. First, do you have any comments on how this endpoint is different and may or may not impact your thinking for the regulatory strategy for SNDX5613? And second, how do you see the targeted MPN1 mutant AML landscape evolving with the potential for multiple therapies available for the population?
spk01: I guess, and thanks so much for your question. So the first has to do with MRD negativity as an endpoint. We give a lot of credit to our competitor who has brought that forward and apparently got an FDA endorsement to use that as an endpoint for accelerated approval in a randomized trial. To our knowledge, that as an endpoint in a single arm trial in a relapsed refractory population is not something the agency has been open to to date, obviously something for further regulatory discussions. So I think that that is probably not something we're going to be able to discuss with EFTA, but we're not counting on that being an endpoint for our relapsed refractory population. But similar to what Dave described, we do think that could be an endpoint in a, let's say, a first-line trial where you use that as your accelerated approval endpoint. I think your second question about the landscape for NPM1 disease, you know, I think there's, you know, obviously we believe that the men inhibition pathway, the men inhibitors are going to be very important agents for those patients. whether there'll be other agents that work for those patients as well, time will tell.
spk02: Got it. And I have one more question. You've mentioned the potential approvals in TGVHD, but I was wondering if you can provide some additional color in your thoughts on the landscape there. Do you anticipate that most of the GVHD patients will end up cycling through all of the available drugs, or do you think that they'll remain on one drug for a long period of time and there'll be a a lot of competition in the first and second line on that front.
spk01: Yeah, it's a good question. You know, I think the landscape in chronic graft-versus-host disease is infancy is sort of evolving. We haven't really had, you know, approved drugs. There's not a defined treatment pathway for patients. So if you go on this one, then that one. We also think that different agents may have, you know, let's say, better efficacy for different manifestations of the disease. So I think it's something that we'll sort of see how that evolves. But, you know, I think we're quite excited to have an agent that shows broad activity against many manifestations of the disease and, of course, is the only one that's targeting macrophages. I think the other part to your question about how this landscape will evolve is are there rational combinations that perhaps even earlier in the treatment course, you could have a more profound effect on the patient's disease.
spk02: Got it. Thanks for taking my questions.
spk08: Thank you. And as a reminder, to ask a question, you'll need to press star 1 on your telephone. Our next question comes from David Liebowitz with Morgan Stanley. You may proceed with your question.
spk07: Thank you very much for taking my questions. Understanding that the numbers are somewhat limited at this point, is there any qualitative insight you can give us as to the effect of 5613 on ALL patients in the study?
spk01: Yeah, I think, David, you're right. The numbers are on the small side. Most of the patients with MLLR that have come in have been AML patients. Again, one of the vignettes that Eitan reviewed at the data disclosure was a patient with what we call mixed phenotypic acute leukemia. Many people bucket that in the ALL bucket. So the numbers are small. I guess I'd say to your question, qualitatively, it looks the same in ALL as it does in AML, but the numbers are small.
spk07: Fair enough. And as far as the NPM1 patients, I guess, how does that 29% response rate look vis-a-vis the response rate for the current standards in the similar treatment population?
spk01: Yeah. So, again, for relapsed refractory acute leukemia, for both NPM1 and MLLR, there really aren't good therapies for these patients. So today, if they're truly relapsed or fractured with either of those mutations, they're generally being treated with chemotherapy. And There's not a lot of really solid data on the response rate for those specific lesions, but overall, if you look in the relapsed refractory population, you'll see a response rate, again, a CR rate for chemotherapy probably no higher than 10%. So, you know, we think that what we're seeing both in NPM1 and in MLLR, again, with a safe oral agent response, is probably quite an excess of what you would anticipate with yet another round of toxic chemotherapy.
spk07: Thanks for taking my question.
spk08: Thank you, and I'm not showing any further questions at this time. I would now like to turn the call back over to Dr. Morrison for any further remarks.
spk01: Great. Thanks very much, Hopper. Thanks, everybody, for joining us on the call today. Again, I think we remain really quite excited about what we're seeing both with 5613 and with acetilumab, and we look forward to presenting additional data in the future. Thank you for joining.
spk08: Thank you, ladies and gentlemen. This concludes today's conference call. Thank you for participating. You may now disconnect.
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